DefinitionThis section has been translated automatically.
Angioedema of the upper airway is a potential life-threatening emergency. For clinical practice, a rough classification according to their etiopathogenesis has proven useful.
ClassificationThis section has been translated automatically.
Classification of angioedema of the head and neck region (varied n. Bas et al. 2013)
- Histamine-mediated angioedema (1%!)
- Non-histamine-mediated angioedema
- acute phase-mediated angioedema
- inflammation-induced angioedema - due to e.g. peritonsillar abscess or acute tonsillitis with accompanying inflammatory reactions (about 79%)
- tumor-induced angioedema (7%)
- bradykinin-induced angioedema (8%)
- idiopathic angioedema (5%)
- acute phase-mediated angioedema
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Clinical featuresThis section has been translated automatically.
Acute-phase edema: Inflammatory edema of the head and neck region represents the most frequent events in a general consultation, accounting for about 80% of all acute edema in this region. Causes are infectious-inflammatory diseases such as peritonsillar abscesses or acute tonsillitis with accompanying inflammatory edema. Painful, usually unilateral protrusion of the soft palate with edema of the uvula occurs.
Bradykinin-induced acquired angioedema: At 8%, these represent the second most common group of acute edemas of the head and neck region. They affect about 30,000 people/year in Germany. Bradykinin-induced angioedema is caused in the vast majority of cases by the use of ACE inhibitors. More rarely, angiotensin type I receptor blockers (sartans) are causative. Bradykinin-induced angioedema occurs predominantly in the first 3 years of use. However, there are also cases in which much longer latency periods (up to 11 years) have been observed.
Histamine-mediated acquired angioedema: quite predominantly in patients with acute or chronic urticaria. Here, the clinical presentation quickly leads to the diagnosis. In classic type I reactions, the relationship between exposure and clinical reaction is usually evident and also remembered by the patient.
Hereditary angioedema (HAE/s.u. Angioedema hereditary; HAE typeI - HAE type VIII)
TherapyThis section has been translated automatically.
Diagnostic pathway for acute angioedema of the head and neck region
- Alerting of an airway team (anesthesiologist, emergency physician)
- Securing the airway (oral pharyngeal examination)
- Where is the angioedema located? (tongue, soft palate, hypopharynx/larynx, face-lip)
Therapy of histamine-induced anigoedema
- Clemastine 2 mg i.v.
- Prednisolone 500 mg i.v.
- If necessary, adrenaline in case of circulatory involvement (0.3-0.5 mg adrenaline i.m.)
Therapy of bradykinin-induced angioedema
- Icatibant 30 mg s.c. (effect after 30 to 45 min)
- alternatively -at present still experimental-: C1-inhibitor concentrate (Berinert P, Cinryze, Ruconest) or administration of a kallikrein inhibitor (Kalbitor)
- if necessary adrenaline in case of circulatory involvement (0.3-0.5mg adrenaline i.m.)
LiteratureThis section has been translated automatically.
- Bas M et al (2013) Angioedema of the head and neck region. Allergo J 22:118-123
- Firazyr. [http://ec.europa.eu/health/documents/community-register/2018/20180426140571/anx_140571_en.pdf EMA SUMMARY OF THE CHARACTERISTICS OF THE MEDICINE]
Outgoing links (5)Ace inhibitors; Angioedema acquired; Angioedema hereditary ; Icatibant; Urticaria (overview);
Please ask your physician for a reliable diagnosis. This website is only meant as a reference.